Archive for January 2014

In our stressed out hyper-driven world of rising global incidence of diabetes, it is always good news to discover evidence that inescapable habits (also known as “well established neural circuits”) can be helpful!

In this case researchers studied over a million coffee drinkers and concluded: “This study provides strong evidence that regular consumption of coffee is beneficial for prevention of diabetes.”

Those who consumed one cup daily demonstrated the best preventative effect with gradual decrease in benefit as the number of cups increases.

Affirmation of the Taoist proverb:

“Everything in moderation, Nothing in excess” (with the possible exception of moderation……)

Coffee, Even Decaf, Linked to Lower Type 2 Diabetes Risk

Nancy A. Melville

January 28, 2014

Coffee consumption is strongly associated with a reduced risk for type 2 diabetes, regardless of whether the coffee is caffeinated or not, according to a new meta-analysis of 28 prospective studies, published in the February issue of Diabetes Care.

“Compared with no coffee consumption…6 cups/day of coffee was associated with a 33% lower risk of type 2 diabetes,” the authors write, adding, “Caffeinated coffee and decaffeinated coffee consumption were both associated with a lower risk of type 2 diabetes.”

Drinking coffee has been well-established in previous meta-analyses as being associated with a reduced risk for type 2 diabetes; however, the new review was needed to account for more recent trials evaluating the benefits of caffeinated vs decaffeinated coffee, the authors explain.

“We found that a 1-cup/day increment of regular coffee was associated with a 9% reduction in diabetes, and 1 cup/day of decaf was associated with 6% reduction in diabetes, but the difference in risk reduction between the 2 types of coffee was not statistically different,” said senior author Frank B. Hu, MD, PhD, a professor of nutrition and epidemiology with the Harvard School of Public Health in Boston, Massachusetts.

“This study provides strong evidence that regular consumption of coffee is beneficial for prevention of diabetes,” Dr. Hu told Medscape Medical News. “For individuals who already drink coffee, they may enjoy this and other potential health benefits, and for those who are sensitive to the effects of caffeine, decaf may confer similar benefits.”

Robust Findings

The 28 studies in the analysis included 1,109,272 participants, and all had the outcome of risk for type 2 diabetes; there were 45,335 cases of diabetes, with follow-up ranging from 10 months to 20 years.

The relative risk for type 2 diabetes with coffee consumption, compared with no or rare consumption, ranged from 0.92 for 1 cup per day, 0.85 for 2 cups, 0.79 for 3 cups, 0.75 for 4 cups, 0.71 for 5 cups, and 0.67 for 6 cups.

Meanwhile, the relative risk for diabetes associated with 1 cup of caffeinated coffee per day (compared to no or rare coffee consumption) was 0.91 compared with 0.94 for 1 cup of decaffeinated coffee per day ( P = .17).

The findings were consistent for men as well as women, and while coffee-brewing methods were not assessed in the studies, the inclusion of diverse populations likely covered a wide array of methods, the authors note.

“Most coffee is likely to be filtered coffee, and the results from studies conducted in various populations, including US, European, and Asian, were similar, indicating consistency of the results despite potentially different preparation and processing methods,” they observe.

And while none of the studies assessed levels of sugar and dairy added to coffee, the amounts are “likely to be small compared with other food sources,” they add.

While this meta-analysis does provide “strong evidence” that higher consumption of coffee is associated with a significantly lower risk for diabetes, “longer-term randomized controlled trials are needed to establish causality and to elucidate the underlying mechanisms,” they conclude.

Coffee Just a Small Part of the Diabetes Equation

One possible explanation for the reduced risk for diabetes with coffee consumption could be the role of chlorogenic acid, a phenolic compound and a major component of coffee, Dr. Hu said.

“Compounds in coffee also include antioxidant polyphenols, minerals such as magnesium and chromium, [and] vitamins; however, it is impossible to tease out the effects of individual compounds, because they don’t exist in isolation in coffee and they may have synergistic effects.”

He stressed also that coffee consumption remains a small piece of the picture.

“Coffee is only one of many dietary and lifestyle factors that can contribute to diabetes prevention. Clearly, maintaining a healthy weight through diet and exercise is the most important way to reduce risk of diabetes. For those who drink coffee regularly, they should enjoy it, but they still need to watch their weight and be physically active.”

The research received funding from the National Institutes of Health. The authors have reported no relevant financial relationships.

This article presents evidence that links a measure of experienced state of well-being generated in the mid-brain (depression) with a metabolic condition (diabetes) and the risk of myocardial infarction (heart attack. All three systems are fed by the vagus (ninth cranial) nerve and can be regulated by mindfulness practices.

Diabetes and Depression Combo Hikes MI Risk

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

BARCELONA — Individuals who have both diabetes and depression have an increased likelihood of having a myocardial infarction (MI), a large Swedish study affirmed.

The odds of having an MI compared with individuals without either condition were greatest among those ages 45 to 64, with the strongest association seen in women (OR 7.1, 95% CI 6.1-8.2), according to Karin Rådholm, of Linköping University in Sweden.

Rådholm and colleagues explored the link between diabetes, depression, and MI using data on 3,738,524 individuals ages 45 to 84 from Swedish national registries of prescription drug use, hospitalizations, and deaths. The analysis excluded those who had had an MI before the beginning of the study period.

Prescriptions for medications for diabetes and depression were used as surrogates for the conditions themselves.

The researchers divided the patients into four groups, which could be shuffled each of the 3 years of the study, based on drug use:

Neither type of medication

Anti-diabetics only

Antidepressants only

Both types of drugs

During the 3-year follow-up, 1.2% of the participants had a first MI. Of those, 37% were fatal.

In the older half of the cohort (ages 65 to 84), all three of the drug groups carried an increased likelihood of having an MI, with odds ratios ranging from just over 1.0 to about 3.0 compared with non-users. The greatest odds were observed in those taking both types of medication and in women versus men.

The findings were similar in the younger half of the cohort (ages 45 to 64), with odds ratios ranging from just over 1.0 to about 7.0. The results were not changed by adjustment for the use of anti-hypertensives.

The findings were not surprising, according to Ewan Pearson, PhD, MBBChir, of the University of Dundee in Scotland. “It’s a very nice, large study that establishes the fact that people with diabetes and people with depression have higher rates of cardiovascular events,” said Pearson, who co-chaired the session at which Rådholm presented the results.

What is noteworthy is the large sample size used in the analysis, he said.

“A study of 3.7 million is incredible,” he said. “It just shows the utility of these massive population resources that Sweden has access to.”

Rådholm acknowledged that the study was limited by the lack of information on the indications for use of antidepressants, noting, for example, that tricyclics can be used for neuralgias and other conditions. The analysis also lacked information on important confounders, such as smoking, lipid levels, and lifestyle.

This article is self explanatory. Note the setting in which the study was done however. Seventh-Day Adventist Communities are atypically more cohesive than those of mainstream Americans. They also have been practicing social values that exemplify, “clean, spiritually intentional living” for several generations. BMI stands for base metabolism index.

Vegetarians Slimmer Than Meat-Eaters, Study Finds

A new study from Loma Linda University researchers shows an association between diet type and weight, with vegetarians having a lower body mass index than non-vegetarians. Interestingly, researchers found this association despite both groups in the study having similar caloric intake.

The Journal of the Academy of Nutrition and Dietetics study is based on data from the Adventist Health Study 2, which includes dietary data from five groups: meat-eaters, semi-vegetarians (occasional meat-eaters), pesco-vegetarians (vegetarians who eat fish), lacto-ovo vegetarians (vegetarians who consume dairy) and vegans (who don’t consume any animal products). Data was collected between 2002 and 2007 from 71,751 Seventh-Day Adventist men and women, with an average age of 59.

Caloric intake was similar among all dietary patterns — about 2,000 calories a day — with the one exception being the semi-vegetarians, who consumed 1,707 calories a day.

Researchers found that average BMI was lowest among vegans, while average BMI was highest among the meat-eaters. Looking specifically at obesity (defined as having a BMI over 30), researchers found that vegans had the lowest percentage of people who were obese — just 9.4 percent — while meat-eaters had the highest percentage of people who were obese — 33.3 percent. About 24 percent of semi-vegetarians were obese, 17.9 percent of pesco-vegetarians were obese, and 16.7 percent of lacto-ovo vegetarians were obese.

Even though calorie intake was similar across all the groups, there were differences in the types of nutrients consumed. Meat-eaters had the lowest intake of plant proteins, beta carotene, fiber and magnesium, and the highest intake of heart disease-linked fatty acids.

Of course, diet isn’t the only factor in weight — the study didn’t examine other factors, such as exercise or socioeconomic status. It merely showed an association between eating patterns and weight, not a cause-and-effect relationship.

More evidence is offered here that given how we measure health, location, income and wealth disparities correlate with a community’s status. The wider the disparity in a community, the lower the health status for all individuals whether more or less economically secure.

This article was downloaded from open source DiabetesPro Smart Brief: (http://www.ledgertranscript.com/home/9046656-95/geographical-location-income-determine-health-care-in-us)

Geographical location, income determine health care in U.S.

Low-income Americans’ access to health care and the quality of care they receive vary widely based on where they live, according to a recent report released by the Commonwealth Fund, a health policy think tank.

Compared to wealthier people, low-income Americans lose more teeth, have more asthma flare-ups and miss out on vaccinations and cancer screenings. They also are less likely to have health insurance.

The report provides a state-by-state comparison of health care for the 39 percent of people with incomes less than 200 percent of the federal poverty level, or $47,000 for a family of four and $23,000 for an individual. Information garnered from the report indicates that we are often two Americas divided by income and geography when it comes to opportunities to lead long and healthy lives.

Statistics drawn from a recent Time Almanac on income disparity notes that low-income people account for at least one-quarter of total state populations, yet account for almost half in some states, i.e. Arkansas, Louisiana, Mississippi and New Mexico.

To understand how many inhabitants of a country are poor, it is not enough to know a country’s per capita income. The number of poor people in a country and the average quality of life depend on how equally or unequally income is distributed across the population, as measured by the Gini index or coefficient. Information drawn from the World Bank indicates that the United States rates 40.8 on the Gini index. The poorest 20 percent of our population receives approximately 5.2 percent of income, while the richest 20 percent receives 46.4 percent of income.

The disparities regarding the quality of health care received by people with low incomes and higher incomes, more than 400 percent of the poverty level, or $94,000 for a family of four was major across the income distribution in each state.

It has been determined that higher-income people in states with low health care scores are often worse off than low-income people in states with high health care ratings. For example, low-income elderly Medicare beneficiaries in Connecticut and Wisconsin are less likely to receive high-risk medications than high-income elderly people in Mississippi, Louisiana and Alabama.

Hawaii and states in the upper Midwest and Northeast had the best scores, while Southern and South Central states often lagged. Among low-income people, there were two- to five-fold differences in their health care and health outcomes scores, depending on where they lived.

Among the other findings:

The percentage of uninsured low-income adults ranged from a low of 12 percent in Massachusetts to a high of 55 percent in Texas.

Only 32 percent of low-income adults aged 50 and older received recommended preventive care, such as cancer screenings and vaccines. Rates ranged from 26 percent or less in Idaho, Oklahoma and California to 42 percent in Massachusetts.

In eight states, 40 percent or more of Medicare beneficiaries received medications considered high risk for the elderly — rates more than double that of states with safer prescribing.

Asthma-related hospitalizations among children from low-income communities in New York were eight times higher than in Oregon, the state with the lowest rate (477 per 100,000 in New York compared to 56 per 100,000 in Oregon).

At least one of four low-income adults under age 65 in West Virginia, Tennessee, Alabama, Mississippi and Kentucky lost six or more teeth due to decay or disease, compared to less than 10 percent in Connecticut, Hawaii and Utah, the states with the lowest rates.

Low-income people were more likely to be uninsured or underinsured than those with higher incomes. In 2010-11, nearly 56 million low-income people were uninsured or underinsured, ranging from a low of 36 percent in Massachusetts to a high of more than 60 percent in Alaska, Colorado, Florida, Idaho, Montana, Nevada, New Mexico, Texas, Utah and Wyoming.

The sharp differences in health care access, quality and outcomes identified in the report result in a substantial loss of lives and missed opportunities to improve health and quality of care.

Using the measurement criteria where all states across the country could provide the same levels of health care accessibility and quality:

Tens of millions of adults and children would receive needed preventive care, such as vaccines, check-ups and cancer screenings.

About 30 million more low-income adults and children would have health insurance, reducing the number of uninsured Americans by half.

About 33,000 more infants born to low-income mothers would survive until their first birthday.

We are talking about people’s lives, health and well-being being affected by income disparity and disparity in the level of medical goods and services availability to all across the country. It is hoped that state policymakers and health care leaders use these data to target resources to improve access, care and the health of residents, especially those with below-average incomes.

This article was downloaded from open source DiabetesPro Smart Brief: (http://www.scienceworldreport.com/articles/12262/20140119/diabetes-prevention-try-a-little-chocolate-tea-and-berries.htm)

A recent study shows how tea, berries and chocolate could all help in the prevention of Type 2 Diabetes due to the high levels of flavonoids.

Based on a study of almost 2,000 people, researchers found that these food groups also help to lower inflammation and insulin resistance.

Professor Aedin Cassidy of the University of Anglia (UEA)’s Norwich Medical School, discusses the study, courtesy of a press release. “Our research looked at the benefits of eating certain sub-groups of flavonoids. We focused on flavones, which are found in herbs and vegetables such as parsley, thyme, and celery, and anthocyanins, found in berries, red grapes, wine and other red or blue-coloured fruits and vegetables.

“This is one of the first large-scale human studies to look at how these powerful bioactive compounds might reduce the risk of diabetes. Laboratory studies have shown these types of foods might modulate blood glucose regulation – affecting the risk of type 2 diabetes. But until now little has been know about how habitual intakes might affect insulin resistance, blood glucose regulation and inflammation in humans.”

For the study, researchers examined close to 2,000 healthy women volunteers from Twins, U.K. who had completed a food questionnaire that estimated their total dietary flavonoid intake as well as six flavonoid subclasses. Blood samples from participants showed evidence of both glucose regulation and inflammation. They also assessed fasting insulin and glucose levels via an equation.

“We found that those who consumed plenty of anthocyanins and flavones had lower insulin resistance. High insulin resistance is associated with Type 2 diabetes, so what we are seeing is that people who eat foods rich in these two compounds – such as berries, herbs, red grapes, wine- are less likely to develop the disease.

“We also found that those who ate the most anthocyanins were least likely to suffer chronic inflammation – which is associated with many of today’s most pressing health concerns including diabetes, obesity, cardiovascular disease, and cancer.

“And those who consumed the most flavone compounds had improved levels of a protein (adiponectin) which helps regulate a number of metabolic processes including glucose levels.”

However, the researchers note that further studies will be needed to potentially determine how the compounds directly lower the risk.

More information regarding the study can be found via the Journal of Nutrition.

(dailyRx News) Fish is commonly referred to as “brain food,” and now research is also showing that it may help prevent some chronic diseases like diabetes.

A recent study found that men who got more than 5 grams of omega-3 polyunsaturated fatty acids — fats that are primarily found in fish and other seafood — per day had a lower risk of developing type 2 diabetes than men who consumed lower amounts.

The authors of this study noted that a more diverse study sample is needed to confirm these findings.

This study was led by Jyrki K. Virtanen, PhD, from the Institute of Public Health and Clinical Nutrition at the University of Eastern Finland in Kuopio, Finland. This research team examined the relationship between omega-3 polyunsaturated fatty acids (PUFA) from fish and type 2 diabetes.

Omega-3 polyunsaturated fatty acids are essential fats that play a role in brain function and growth and development, but the body does not produce these fats. They must be consumed in the diet.

Dr. Virtanen and colleagues analyzed data from 2,212 men in the Kuopio Ischaemic Heart Disease Risk Factor study. These men, who were between the ages of 42 and 60 years old, did not have type 2 diabetes at the beginning of the study between 1984 and 1989.

The researchers looked at intake of four types of omega-3 polyunsaturated fatty acids. Serum polyunsaturated fatty acid levels were measured from blood samples to determine levels of exposure to polyunsaturated fatty acid levels.

The participants were instructed to record what they ate for four days, and their records were run through a nutrition software program to determine the nutrients present in the foods they ate. They were separated into four groups depending on the amount of omega-3 polyunsaturated fatty acids they consumed ranging from lowest (less than 3.62 grams per day) to highest (more than 5.33 grams per day).

Type 2 diabetes status was determined through a combination of self-report, a fasting plasma glucose test (measures blood sugar levels) and an oral glucose tolerance test (measures how well the body breaks down glucose) at 4, 11 and 20 years after the study began.

The researchers accounted for several factors that could have influenced the development of type 2 diabetes, including medical history, medication use, family history of diabetes, smoking status, alcohol consumption, blood pressure, body mass index (a measure of height and weight), education and annual income.

The researchers found that during the follow-up period, about 19 percent of men developed type 2 diabetes.

Study participants who consumed more than 5.3 grams per day of three of the types of omega-3 polyunsaturated fatty acids — eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) — had a 33 percent lower risk of type 2 diabetes than men who consumed less than 3.62 grams per day.

The fourth type of omega-3 polyunsaturated fatty acid — alpha-linolenic acid (ALA) — was not found to be related to diabetes risk.

Since fish can contain high levels of mercury, which has been linked to a higher risk for cardiovascular diseases, the researchers also measured hair mercury levels to determine the relationship between mercury levels and risk of type 2 diabetes. The researchers did not find a relationship between hair mercury levels and risk of type 2 diabetes.

The study’s authors concluded that omega-3 polyunsaturated fatty acids appeared to be connected to a lower risk of type 2 diabetes, but research is needed in more diverse populations to confirm this finding.

This open source Medscape (http://www.medscape.com/today) article discusses research that affirms the neurogenerative effects of regular mindfulness-based stress reduction (MBSR) practice. “Time in” makes for more present time out in the world!

Meditation in patients with mild cognitive impairment (MCI) may slow progression to Alzheimer’s disease (AD), new research suggests.

A small, randomized pilot study of adult patients with MCI showed that those who received mindfulness-based stress reduction (MBSR) therapy for 8 weeks had a greater increase in functional connectivity between brain regions related to both MCI and AD than those who received usual care.

These regions included the posterior cingulate cortex, the bilateral medial prefrontal cortex, and the left hippocampus.

In addition, there was “a trend” toward less bilateral hippocampal volume atrophy in the patients who received MBSR compared with the usual-care group.

“This study suggests that an intervention with meditation and yoga may impact the areas of the brain that are most susceptible to developing dementia,” lead author Rebecca Erwin Wells, MD, MPH, who was at Beth Israel Deaconess Medical Center (BIDMC) at Harvard Medical School in Boston, Massachusetts, at the time of the study, told Medscape Medical News.

Dr. Wells, who is now an assistant professor in the Department of Neurology at Wake Forest Baptist Medical Center in Winston-Salem, North Carolina, noted that although this was a small, preliminary study, she is “very excited” about the findings.

“MBSR is a relatively simple intervention, with very little downside, that may provide real promise for these individuals. If [it] can help delay the symptoms of cognitive decline even a little bit, it can contribute to improved quality of life,” said Dr. Wells in a release.

The study is scheduled to be published in the November 27 print issue of Neuroscience Letters.

No Current Treatment

The investigators note that patients with high stress levels are at increased risk of developing MCI and AD, and more than 50% of those with MCI will go on to develop dementia within 5 years.

“Despite the clinical and public health significance of MCI, there are no known therapies preventing progression to dementia,” they write.

“While meditation may reduce stress and alter the hippocampus and default mode network (DMN), little is known about its impact in these populations.”

“We were particularly interested in looking at the DMN, the brain system that is engaged when people remember past events or envision the future, and the hippocampus, the part of the brain responsible for emotions, learning, and memory,” said Dr. Wells.

She added that they wanted to investigate whether MBSR could attenuate the decline of individuals already experiencing memory problems.

A total of 14 adults older than 54 years with MCI were enrolled between 2010 and 2011 and were randomly assigned to receive either MBSR (n = 9; mean age, 73 years) or usual care (control group; n = 5; mean age, 75 years).

MBSR teaches both mindfulness meditation and yoga. Those who received this arm of treatment underwent 8 weekly 2-hour sessions plus 1 “mindfulness retreat day.” In addition, this group was encouraged to spend 30 minutes a day listening to guided audio recordings in their own homes.

All participants also underwent resting state functional magnetic resonance imaging (fMRI) at baseline and at the 8-week mark to measure connectivity changes in areas of the DMN. And MRIs were conducted to measure volume changes in the bilateral hippocampus.

This is “the first study to our knowledge reporting the impact of MBSR on fMRI among patients with MCI,” the researchers write.

Increased Connectivity, Less Atrophy

Results showed that, compared with the control group, the MBSR group had a significantly greater increase in functional connectivity between the posterior cingulate cortex (PCC) and the bilateral medial prefrontal cortex and between the PCC and the left hippocampus, as shown by fMRI scans.

Both treatment groups showed bilateral hippocampal atrophy from baseline to the 8-week follow-up, as shown in the MRI scans. Still, although not statistically significant, there was a trend toward less volume atrophy in the MBSR group (P = .07).

No study-related adverse events were reported by either group.

“MBSR may affect the region of the brain most sensitive to MCI and AD,” write the investigators.

“If some component of cognitive decline is a function of stress-induced hippocampal changes, then meditation may impact the hippocampus as a stress-reducing technique thereby improving cognitive reserve,” they add.

The researchers note that more studies with larger sample sizes and longer follow-up periods are now needed, but they voiced optimism in the findings of their small trial.

“For a condition without a standard treatment and with potential progression to AD, this study provides preliminary evidence that an intervention with limited side effects may be of potential benefit to patients with few other options for improvement,” they write.

Dr. Wells noted that researchers at both BIDMC and Wake Forest are continuing to examine these issues.

Durable Effect?

“I think this study offers a very useful component of therapy for these patients, for several reasons,” David Geldmacher, MD, professor and Patsy and Charles Collat Scholar in Neuroscience in the Division of Memory Disorders and Behavioral Neurology at the University of Alabama at Birmingham, told Medscape Medical News.

“First, we know that it’s a stressful experience for people with the illness, especially in the early stages. So anything that can help to address that frustration on a symptomatic level is important,” said Dr. Geldmacher, who was not involved with the study.

He added that a sense of control and self-direction “is crucial” in this patient population.

“This is an illness where people often feel that someone else is starting to drive the bus and that the disease is starting to take away their rights and privileges. So the ability to do something themselves that may potentially alter the course of their illness is important,” he said.

Dr. Geldmacher noted that the physiologic part of this study was also interesting.

“What we don’t know in as much detail is whether this intervention could have an ongoing, clinically meaningful effect or not. Obviously there’s going to be very little harm, if any, to doing this, and we get the psychological benefits,” he said.

“So even if meditation did nothing to the hippocampal structure, it may help to reduce the symptom burden of the illness as a whole.”

Can’t Hurt, May Help

Thaddeus W. W. Pace, PhD, assistant professor in the College of Nursing and the Department of Psychiatry, College of Medicine, at the University of Arizona in Tuscon, told Medscape Medical News that he had some concerns with the research, including that it was a pilot study and that there were so few participants.

“Even for an imaging study, the number was on the lower side. Also, the overall design could have been a little stronger,” he said. For example, he questioned the use of treatment-as-usual for the control condition instead of an active control condition in which participants would also meet with others during the course of the study.

“This would account for the social contact that happens during meditation training. One of the most important challenges we have in our research is how we design the control condition that we’re comparing everything to.”

Dr. Pace, who was not involved with this study, has conducted previous research examining the effects of meditation on the brain’s response to emotional stimuli.

He went on to note, however, that the current study “does have some exciting points.”

“The findings themselves are pretty cool, and the outcomes make me want to know more. The big finding was about the [DMN] areas and how they’re all working together. And that was quite fascinating,” said Dr. Pace.

“The hippocampal volume outcome, even though it was a trend, was also pretty exciting to me, especially because my interest is in stress and health. We know that stress response and inflammation have an impact on chronic illnesses, including Alzheimer’s,” he explained.

“When the hippocampus atrophies, it may lead to inappropriate regulation of the stress response systems, which can then further the illness process. So it was very interesting that MBSR had an impact, or at least a trend, on hippocampal volume in these folks with MCI.”

Overall, Dr. Pace said that it appears that MBSR could be beneficial to this patient population.

“As long as you tell patients that this study’s findings are preliminary, I would be comfortable recommending to clinicians that they recommend MBSR to their patients,” said Dr. Pace.

“It can’t hurt, and as a program, it could only be helpful. If a patient has enough time to devote to it, why not try it? And then clinicians should also keep an eye out for the next-generation study.”

The study was funded by several grants and sources, including the National Institutes of Health National Center for Complementary and Alternative Medicine. A full list of funders is available in the original article. The study authors and Dr. Pace have disclosed no relevant financial relationships. Dr. Geldmacher also has disclosed no relevant financial relationships, but he did report that Dr. Wells was a former student of his.

Here is a compelling discussion about the relationship between dietary carbohydrates and dementia. Once again,gluten is implicated but not the sole potential culprit.

This interview was posted on the open source Medscape website.http://www.medscape.com/today

Dementia: Is Gluten the Culprit?

Bret S. Stetka, MD, David Perlmutter, MD

DisclosuresJanuary 21, 2014

Editor’s Note:In his new book Grain Brain: The Surprising Truth About Wheat, Carbs, and Sugar — Your Brain’s Silent Killers, Dr. David Perlmutter, Associate Professor at the University of Miami School of Medicine, advocates that lifestyle modifications, starting with a high-fat, nearly carbohydrate-free diet, can prevent or greatly lower dementia risk and progression — and he’s armed with plenty of data to back up the claim. But detractors say the evidence isn’t quite there. With Grain Brain about to hit its 15th straight week on the New York Times best-seller list (including a stint at the top spot) Medscape spoke with Dr. Perlmutter about his thoughts on the impact of carbohydrates and gluten on the brain.

Medscape: For those unfamiliar with your ideas, can you summarize the thesis behind your new book and how you arrived at it?

Dr. Perlmutter: Certainly. I’m a board-certified neurologist and a fellow of the American College of Nutrition. I’ve been very frustrated with neurology over the past 20 years, because we’re trained in residency and practice to basically treat symptoms of neurologic disorders. I found that not to be satisfying and thought it was important to delve into causality as opposed to just focus on treating the smoke and ignoring the fire.

That said, with time we began seeing wonderful research citations that were drawing a link between risk for dementia, for example, and blood sugar levels appearing in our most well-respected journals. For example, a study published in Neurology in 2005[1] pointed a finger squarely at the most powerful metric being glycated hemoglobin. Even back then, it was becoming clearer that there was something going on with blood sugar correlating with rate of brain atrophy, specifically hippocampal atrophy, and cognitive decline. When you now retrospectively evaluate that study, you begin to appreciate that glycated hemoglobin is more than just a metric of average blood sugar, which is typically how it’s looked upon even today.

Glycated hemoglobin is a glycated protein. This is a marker not just of average blood sugar, but more important, it’s a marker of the degree of glycation that’s going on in human physiology — a process that increases inflammation and dramatically increases the production of free radicals and oxidative stress. So the idea that even subtle elevations of sugar, which is a dietary lifestyle choice, are related to risk for brain degeneration really began to crystallize.

This notion has gained traction and, I think, is profoundly supported by a couple of more recent studies. A study published in August 2013 in the New England Journal of Medicine (NEJM)[2] was very supportive, indicating that even subtle elevations of fasting blood sugar translates to dramatically increased risk for dementia. This was a prospective analysis that measured fasting blood sugar and followed 839 men and 1228 women for a mean of 6.8 years. I’ll quote the conclusion: “Our results suggest that higher glucose levels may be a risk factor for dementia, even among persons without diabetes.”

Why? These are levels of 105 and 110 mg/dL — levels that most doctors are going to be satisfied with. However, according to the study, these numbers translated into a significantly increased risk for dementia in individuals who were not demented.

Medscape: That is striking. However, I think it’s important to point out that many of the studies you cite report associations between glucose and risk for dementia and don’t necessarily prove causality, correct?

Dr. Perlmutter: You are 100% correct. I’ll stand and take my lumps from those individuals who want to make the argument that there’s no smoking gun here. But when a prestigious journal like NEJM calls our attention to this relationship effect in glucose and cognitive decline, we’ve got to take notice, especially at a time when we have no other choice. It’s the best thing that we have going.

We know that a lower-carbohydrate diet is the right choice for the heart and the immune system. There’s no downside to it. I offer it up as being supported by the current peer-reviewed literature. If that’s as good as it gets, that’s the best we have right now.

You can wage criticism that the NEJM study was not interventional. It wasn’t a double-blind study testing some sort of pharmaceutical intervention. It was a prospective study that basically asked who’s going to get dementia on the basis of fasting blood sugar levels.

Some people criticize prospective or even retrospective studies because they’re not interventional. I tend to think that they can provide very, very valuable information. There’s never been an interventional trial that’s demonstrated that seatbelts are effective in reducing injuries in a car accident.

The Dementia Diet

Medscape: What type of diet or interventions do you recommend to prevent or slow dementia?

Dr. Perlmutter: The data show that individuals with lower blood sugar levels have a lower risk for dementia. Therefore, we’ve got to keep blood sugar low. We do so by using the time-honored dietary intervention of a lower-carbohydrate, higher-fat diet.

This is what the scientists have told us for years is the best way to lower blood sugar. If you look at the A TO Z trial,which was published in JAMA in 2007,[3] dramatic reductions in blood sugar were seen in participants on a lower-carb, higher-fat diet.

A similar article was published in NEJM in 2008.[4] This was an interventional trial demonstrating both weight loss and reduction of fasting blood sugar in individuals eating a higher-fat, lower-carbohydrate diet.

The Mayo Clinic published a study[5] in the Journal of Alzheimer’s Disease in 2012 demonstrating that in individuals favoring a high-carb diet, risk for mild cognitive impairment was increased by 89%, contrasted to those who ate a high-fat diet, whose risk was decreased by 44%. Drs. Barnes and Yaffe from the University of California, San Francisco, published a study in Lancet Neurology in 2011[6] indicating that about 54% of cases of Alzheimer disease in the United States could have been prevented with attention to lifestyle changes, such as exercise, weight loss, and controlling hypertension.

This province of lifestyle modification in neurologic diseases has not been one of comfort for neurology in general. We neurologists are acting in an essentially reactionary manner. In other words, we are responding to illnesses by hoping that there are medications to treat symptoms, whereas we really ought to embrace the notion of preventive medicine, because the science is staring us in the face.

Medscape: One of the points in your book I found interesting is that you’re not just talking about processed carbohydrates or sugars here, right? You believe that whole grains — typically presumed healthy — also increase dementia risk?

Dr. Perlmutter: Yes, they do. There’s a lot of very good information provided on the glycemic index of these foods. That is a metric of not only just the elevation of blood sugar and the consequence of consuming a particular food, but actually it’s also a measurement of how long the blood sugar remains elevated.

The glycemic index measures what the blood sugar is between 90 and 120 minutes after consuming a particular food. When you look at the glycemic index of whole-grain bread, for example, it’s extremely high: 72-74. It’s higher than that of white bread. It’s much higher than that of many candy bars. It becomes a huge issue in terms of how long your blood sugar remains elevated — that is, how long you have increased risk for glycation of proteins. It becomes a big issue that we have to reconsider these recommendations about whole grains in terms of the simple fact of looking just at the glycemic index.

Medscape: Does the same go for other grains common in health foods these days, such as flax and quinoa?

Dr. Perlmutter: Flax and quinoa (which by definition is actually not a grain) are gluten-free foods rich in fiber and healthful fat. However, they do contain modest amounts of carbohydrate, and assessing these foods by evaluating their glycemic indices will help decide how healthful they really are.

Giving Up Gluten, and the Paleo Diet Fad

Medscape: Why do you feel that gluten is particularly detrimental to our brain health?

Dr. Perlmutter: Gluten-containing foods stimulate inflammatory reactions in a significant number of individuals, well beyond the 1.8% of the population that has celiac disease. This may lead to increased bowel permeability and even increased blood/brain barrier permeability, as described by Dr. Alessio Fasano (formerly at the University of Maryland, now at Harvard).[7] The mechanism deals with the expression of the protein zonulin brought on by gluten exposure. What is so compelling about this newer research is the fact that this reaction to gluten may occur in all humans.

This may explain to some degree the array of neurologic issues now correlated with gluten sensitivity in nonceliac patients, as described by Dr. Anna Sapone and colleagues.[8] So we have to look at gluten sensitivity in a new light, recognizing that its manifestations may extend well beyond the gut. Writing in the Journal of Neurology, Neurosurgery & Psychiatry,[9] Dr. Marios Hadjivassilou stated, “That gluten sensitivity is regarded as principally a disease of the small bowel is a historical misconception. Gluten sensitivity can be primarily and at times exclusively a neurological disease.”

That said, many people shop the gluten-free aisle of the grocery store, thinking that those gluten-free breads, pastas, pizza doughs, crackers, and so on are much better because they’re gluten-free. The bottom line is these are still powerful sources of carbohydrates.

Even fruit is a source of aggressive carbohydrate in the human diet. Take a simple 12-ounce glass of freshly squeezed orange juice — what could be better, right? As a matter of fact, that’s about 34-36 grams of pure carbohydrates. That’s 9 teaspoons of pure sugar with breakfast before your breakfast cereal has even arrived.

My recommendation is to try to keep the total carbohydrates per day to 60-80 grams. If you have 2 glasses of orange juice, you’ve already consumed 72 grams of pure carbohydrate.

It’s really fundamentally important that we address this mechanism of glycation of proteins as being a cornerstone of brain degeneration pathology, and recognize that beta-amyloid itself is a protein that can become glycated and as such can become a powerful nexus for the production of free radicals in inflammation.

We have watched with dismay over the past several years the failure of the drugs designed to rid the brain of beta-amyloid. Most recently, as published in NEJM,[10] a higher dosage of the experimental drug semagacestat was associated with increased cognitive decline of individuals compared with placebo.

Medscape: How does your diet compare with the paleo diet — the idea that we should be following the presumed diet of Paleolithic humans?

Dr. Perlmutter: They are very similar. It’s basically focused on very low carbohydrates and the aggressive addition of good fats: by all means, avoiding modified fats, trans fats, and hydrogenated modified fats, but welcoming back to the table such things as extra virgin olive oil, nuts, seeds, and grass-fed beef (not typical beef).

My diet is not a big beef, go out and eat a lot of meat, kind of diet. When Drs. Campbell and Campbell published The China Study[11] about the possible health consequences of eating meat, their report was valid because by and large, the type of meat that people are eating is derived from animals that have been fed genetically modified corn and soy and high levels of omega-6 fatty acids, which are proinflammatory. Therefore, clearly the idea that there’s a relationship between that type of meat consumption and cardiovascular disease, and even cancer, is valid.

We’re talking about specifically small amounts of grass-fed beef and wild fish. We’re moving the meat, chicken, and fish away from being the centerpiece of the meal to being the side dish, the garnish. Lots of above-ground leafy green vegetables, colorful vegetables, and welcoming back good fats, because that’s what the brain is desperate for.

Medscape: So, it’s in line with a review published by the American Society for Nutrition[12] last year, as well as other recent data[13] suggesting that a little saturated fat, particularly from free-range red meat, might not be so bad for our brain health and may protect against anxiety and depression?

Dr. Perlmutter: Absolutely. And not just from grass-fed beef, but from the dreaded egg as well. There is no relationship in the current peer-reviewed literature between egg consumption and cardiovascular risk — none whatsoever. Yet, there is still the ubiquitous egg-white omelet on every restaurant menu that you can find.

Diet Isn’t Everything

Medscape: There are a lot of data on other lifestyle factors with benefits in dementia — physical activity and mental and social stimulation in particular. How much weight do you give these nondietary factors?

Dr. Perlmutter: We were all over exercise in Grain Brain. One of the notions that I think is very, very empowering and compelling is the idea of neurogenesis — that humans retain the ability to grow new neurons in the hippocampus throughout our entire lifetime. We can enhance our ability for this activity through the process of epigenetics.

A study published in Proceedings of the National Academy of Sciences in 2011 showed that we can actively modify the gene for the production of brain-derived neurotrophic factor (BDNF) with simple exercise.[14] The investigators looked at 120 elderly nondemented individuals over a 1-year period who either stretched or did aerobics. They measured 3 variables: serum BDNF levels, memory function, and morphometric analysis of hippocampal size on MRI before and after the intervention period. After 1 year, the group that did the aerobic exercise had an increase in hippocampus size by about 1%, improvement of memory function, and higher levels of serum BDNF.

What is so incredible about that is there is no pharmaceutical that can do that. Believe me, you would have probably the world’s most valuable pharmaceutical if you could develop a drug that would do that. Plain old physical exercise, nonproprietary. No one owns it. That’s why you don’t hear about this on the evening news. It’s not advertised in our medical journals. Just aerobic exercise improved memory, grew the hippocampus, and raised BDNF levels — which beyond neurogenesis also stimulates neuroplasticity, which is fundamental for learning. How incredible that you can modify the growth of your brain today by engaging in aerobic exercise! All you need to go out and buy is a pair of sneakers.

The Obama administration just dedicated $33 million to help pharmaceutical companies develop an Alzheimer disease prevention pill, and yet this article has already been published showing preservation of hippocampal size and function — in fact, regeneration of hippocampal size and function.

A Whole-Grain Gripe

Medscape: What do you say to the fact that many global diets proven to be healthy — particularly the Mediterranean diet, which is continually shown to be beneficial in numerous medical and mental conditions — include whole grains? And that many of the world’s so-called “blue zones” — regions in which residents have notably long lifespans — also include grains in their diets?

Dr. Perlmutter: I think people do tolerate some amount of grains, and that the classic Mediterranean diet is one that has added fat and lower carbs. Of note, an April 2013 article in NEJM [15] compared a standard US diet with a Mediterranean diet supplemented with extra-virgin olive oil and a Mediterranean diet supplemented with mixed nuts. The investigators looked at 3 endpoints: myocardial infarction, stroke, and death. They had to stop the study halfway through it, at 4.6 years, because the individuals with the highest fat consumption had a 30% lower risk for the endpoints. It was unfair to the rest of the participants.

Can people get away with having some whole grain products? I suspect so. But you have to understand that wheat products represent 20% of our caloric intake in the United States. That’s not the way it is around the rest of the world. The Mediterranean diet, for example, does not pound people over the head with soda.

Medscape: How would you respond to your detractors that there just isn’t enough evidence to support would could be considered a somewhat extreme change in our country’s dietary habits?

Dr. Perlmutter: My response is that the “extreme change in dietary habits,” to quote you, is actually what has happened to human nutrition in only the past several centuries. In the early 19th century, Americans consumed just over 6 pounds of sugar each year. That figure now exceeds 100 pounds. And there has been a dramatic reduction in the consumption of healthful fat. Beyond the mechanism of protein glycation, as well as the powerfully detrimental downstream effects of uncontrolled insulin signaling, we haven’t even begun to understand the epigenetic consequences related to the effects of these new dietary challenges in terms of maladaptive genetic expression.

So in reality, I am not suggesting a change. I am recommending that we end this grand experiment and return to a diet that isn’t evolutionarily discordant.

Medscape: Do you have any final comments for Medscape’s audience of clinicians? How do you feel your ideas should be incorporated into patient care?

Dr. Perlmutter: Again, look at A1c in a different way. Rather than simply representing a metric of average blood sugar over a 3- to 4-month period, look at it as a way of modifying your pharmaceutical intervention; look upon it as a marker of what it really is, glycation of protein. That glycation of protein dramatically relates to inflammation and oxidative stress. That’s number one.

Second, begin to incorporate a fasting insulin metric as a way of anticipating who’s going to then develop elevations of fasting blood sugar and glycation of hemoglobin moving forward. The earliest sign of pancreatic stress is elevation of fasting insulin — which ideally should be less than 8, not up to 24, which is what is in the so-called normal range.

Third, recognize that vitamin D is a powerful player in terms of brain health. Beyond strong and healthy bones, vitamin D activates more than 900 genes in human physiology, most of which are important for brain health. Low levels of vitamin D correlate with increased risk for multiple sclerosis, dementia, and Parkinson disease. Those are my 3 take-home messages.